Male infertility and testicular cancer are thought to result from disruptions to testis development in utero. Physiological perturbations during human pregnancy can feature high activin A levels, and this study investigates how elevated activin signalling affects the cells destined to form sperm. After birth, testicular germ cells resume proliferation and transform into either differentiating spermatogonia that initiate the first round of spermatogenesis, or into spermatogonial stem cells (SSCs) that maintain spermatogenesis in adults. We studied a mouse model with elevated activin A bioactivity (Inha KO; lacks the inhibin a subunit, a potent activin inhibitor), to determine whether this affected establishment of spermatogonia or SSCs. Immunofluorescent analysis was used to score germ cell populations; spermatogonia (marked by SALL4+), nascent SSCs (GFRA1+) and proliferating cells (Ki67+) in Inha WT and KO mouse testis sections at P0, P3 and P6. We discovered that Inha KO testes at P0 have 50% fewer germ cells, indicating vulnerability to elevated activin A during fetal life. Of the remaining germ cells, a higher proportion were GFRA1+ and Ki67+, suggesting advanced development. At P6, when the SSC population is fully established, we observed a higher proportion of GFRA1+ cells in Inha KO testes indicating that elevated activin A favours SSC formation. RNAseq analysis of P0, P3, P6 whole testis samples confirmed transcripts associated with SSCs (Gfra1, Id4, Etv5, Bcl6b, Chd4) and differentiated spermatogonia (Sohlh2, Dnmt1) were elevated in Inha KO testes. This further indicates accelerated/altered spermatogonial development occurs in high activin conditions; whether this is indirect or direct is under investigation using cultured spermatogonia. These new data, showing systemic activin A levels determine the pace of germ cell development and stem cell establishment, suggest that human pregnancy conditions with elevated activin A can influence the male germline and consequently may affect adult fertility.